The host T cell germinal center (GC) derived B lymphoma cell interaction will be examined. A central question to be answered about the lymphomagenesis in SJL mice is: What causes the high mtv-29 encoded vSAg transcription and how does it relate to the GC origin of these lymphomas (RCS)? The 5' LTR of mtv-29 in liver and RCS DNA will be sequenced to determine whether the 5'LTR is defective in all cells or only in RCS cells to explain that the vSAg initiation site is in the end region mtv-29. Regulation of the expression of this vSAg will be studied by using transection of reporter constructs and looking for specific binding factors for regions in mtv-29, expressed in RCS and normal GC but not in other B cells. The mechanism of the growth promotion in vivo will be studies, including the fate of vbeta16+ T cells in c57L mice will be analyzed. The vbeta16 T cell representation in PBL of mice with developing primary lymphomas will be followed and the effect of anti-vbeta16 on tumor growth in vivo evaluated. Attempts will be made to identify secondary oncogenic events that cause continued proliferation and a lack of differentiation in e lymphoma cells. It will be determined whether RCS, normal isolated GC and NJ101 cells differ in resistance to spontaneous and glucocorticosteroid induced apoptosis. The expression of several oncogenes in morphologically abnormal and normal GCs from bcl-2 transgenic and normal SJL mice will be studies. To evaluate whether the phenomenon of ~reverse immune surveillance~ may be applicable to humans, CD4+ T cell infiltrates in human GC-derived lymphomas will be examined for Vbeta or Va TCR patterns that might reflect monoclonal responses to specific Ag or v beta restricted responses to a SAg.